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- W2271136467 abstract "Graft-versus-host disease is a complication in patients undergoing hematopoietic stem cell transplantation. Graft-versus-host disease includes acute graft-versus-host disease and chronic graft-versus-host disease. Host APCs (e.g., dendritic cells and macrophages), effector T cells (e.g., Th1, Th17, and abnormal Th17:regulatory T cell ratio), B cells, and NK cells are implicated in graft-versus-host disease physiopathology. Proinflammation cytokines (e.g., IL-17, IL-1β, and TNF-α) are increased in graft-versus-host disease . Costimulatory molecules play an important role in inducing graft-versus-host disease . Pattern-recognition receptors, such as TLRs and nucleotide-binding oligomerization domain-like receptors, are critically involved in the pathogenesis of graft-versus-host disease . Complement system C3 mediates Th1/Th17 polarization in human T cell activation and skin graft-versus-host disease. Accumulation of CD26 T cells in graft-versus-host disease target organs was found. As a therapeutic target, soluble CD83 molecules or antibodies have been demonstrated to have therapeutic effects against graft-versus-host disease, and signaling molecules promote the inflammatory and immune process of graft-versus-host disease . These immune cells and molecules could be the predictors of graft-versus-host disease development and the drug targets of the treatments for graft-versus-host disease. This article focuses on major advances on cellular and molecular mechanisms in graft-versus-host disease." @default.
- W2271136467 created "2016-06-24" @default.
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- W2271136467 date "2015-12-07" @default.
- W2271136467 modified "2023-10-18" @default.
- W2271136467 title "Cellular and molecular mechanisms in graft-versus-host disease" @default.
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- W2271136467 doi "https://doi.org/10.1189/jlb.4ru0615-254rr" @default.
- W2271136467 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26643713" @default.
- W2271136467 hasPublicationYear "2015" @default.
- W2271136467 type Work @default.